Alcohol consumption induces abnormal alternative splicing events. That is, in tightly controlled experiments, alcohol use has shown to alter the combinations of protein coding (exons) and non-coding (introns) regions in particular transcripts as well as modify the expression of individual gene isoforms relative to naïve controls in brain tissues and cell types3,4. These data suggest that alcohol exposure might directly disrupt alternative mRNA splicing in specific genes. Post-mortem human brain studies identify alternative splicing associations with alcohol use disorder (AUD) highlighting specific gene isoforms among ion channels5 and neurotransmitter receptors6 as well as intracellular pathways and synaptic plasticity processes7. One study reported that AUD causes changes in mRNA splicing in the brain7, but did not explore the possibility of genetic influences, which would be inconsistent with causality.
